Chronic wounds are open to the environment and are susceptible to contamination by bacteria, potentially leading to infection. Some of the consequences of a chronic wound infection are tissue breakdown, pain, additional impedance of the healing ability of the wound, amputation (e.g. in a diabetic foot ulcer) and systemic infection, which can be life-threatening. Identifying infection in chronic wounds is challenging because current clinical practice employs using clinical signs and symptoms (‘NERDS’) (Sibbald et al., Adv. Skin Wound Care 2006; 19(8): 447-61), which are not necessarily distinct from other conditions, such as chronic inflammation. Gardner et al., Ostomy Wound Manage. 2001; 47(1): 40-7. Bacteria and their proteases can stimulate a pro-inflammatory host response and, eventually, clinical signs due to this inflammatory response and tissue damage may be seen (FIG. 1). McCarty et al., Wound Repair and Regeneration 2012; 20: 125-36.
The host response often includes elevated inflammatory markers, e.g. cytokines including tumour necrosis factor alpha (TNFα) and interleukin-1 beta (IL-1β). Unfortunately, clinical signs may not be apparent if the inflammatory response is impaired or defective (e.g. when other co-morbidities are present, such as diabetes or immunosuppressive conditions), thereby increasing the risk of infection. Bacteria are in a pathogenic state when they are either in the process of, or they are capable of, causing disease, i.e. infection. One indication of pathogenicity is the production of enzymatic virulence factors or bacterial proteases. Bacterial pathogenesis is undesirable since, at this stage, the wound is in a part of the wound infection continuum that typically requires intervention (FIG. 6).